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Kang Wang,1,* Zihui Yang,1,* Boyu Zhang,1,* Song Gong,2 Yiping Wu1 1Department of Plastic and Cosmetic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China; 2Division of Endocrinology, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, People’s Republic of China*These authors contributed equally to this workCorrespondence: Song Gong, Division of Endocrinology, Tongji Hospital, Tongji Medical College, Wuhan, Hubei, People’s Republic of China, Email gongsong@tjh.tjmu.edu.cn Yiping Wu, Department of Plastic and Cosmetic Surgery, Tongji Hospital, Tongji Medical College, Wuhan, Hubei, People’s Republic of China, Email tongjiplastic@163.comAbstract: Wound healing in diabetic patients is frequently hampered. Adipose-derived stem cell exosomes (ADSC-eoxs), serving as a crucial mode of intercellular communication, exhibit promising therapeutic roles in facilitating wound healing. This review aims to comprehensively outline the molecular mechanisms through which ADSC-eoxs enhance diabetic wound healing. We emphasize the biologically active molecules released by these exosomes and their involvement in signaling pathways associated with inflammation modulation, cellular proliferation, vascular neogenesis, and other pertinent processes. Additionally, the clinical application prospects of the reported ADSC-eoxs are also deliberated. A thorough understanding of these molecular mechanisms and potential applications is anticipated to furnish a theoretical groundwork for combating diabetic wound healing.Keywords: diabetes, wound healing, ADSC-exos, tissue regeneration, skin cells, inflammation

Xiaoling Zhang,1,2 Jing Tao,1,2 Song Gong,1,2 Xuefeng Yu,1,2 Shiying Shao1,2 1Division of Endocrinology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, People’s Republic of China; 2Branch of National Clinical Research Center for Metabolic Diseases, Wuhan, Hubei Province, People’s Republic of ChinaCorrespondence: Shiying Shao, Division of Endocrinology, Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology, Jiefang Road 1095, Wuhan, Hubei Province, 430030, People’s Republic of China, Email shaoshiyingtj@163.com

Xiaoling Zhang,1,2 Jing Tao,1,2 Song Gong,1,2 Xuefeng Yu,1,2 Shiying Shao1,2 1Division of Endocrinology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, People’s Republic of China; 2Branch of National Clinical Research Center for Metabolic Diseases, Wuhan, Hubei Province, People’s Republic of ChinaCorrespondence: Shiying Shao, Division of Endocrinology, Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology, Jiefang Road 1095, Wuhan, Hubei Province, 430030, People’s Republic of China, Tel +86-13627144576, Fax +86-27-83662883, Email shaoshiyingtj@163.comBackground: Diabetic lower extremity ulcer, including diabetic foot ulcer (DFU) and leg ulcer, is one of the refractory complications of diabetes, the treatment of which is challenging, expensive, and lengthy. Recombinant Human Granulocyte/Macrophage Colony-stimulating Factor (rhGM-CSF) is an immunomodulatory cytokine that has been mainly applied in the treatment of hematological diseases. Clinical evidence regarding GM-CSF in the treatment of diabetic lower extremity ulcers is limited. This study is the first case series that investigates the repurpose effects of rhGM-CSF on diabetic ulcer healing in real clinical practice.Methods: Nine patients diagnosed with diabetes and refractory lower extremity ulcer (ulcer duration ≥ 2 weeks) were included from September 2021 to February 2023 in the Division of Endocrinology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology. Patients with Wagner grade ≥ 4 and SINDAD ≥ 5 were excluded. The included subjects were treated with rhGM-CSF plus standard of care (SOC) including glycemic control, foot care education, debridement of necrotic tissues, topical wound dressings, offloading, and infection control when necessary. The observation endpoint was complete epithelialization. Their clinical manifestations, laboratory tests, and therapeutic

Bo Wang,1,* Song Gong,2,* Lizhi Han,2 Wenkai Shao,2 Zilin Li,2 Jiawei Xu,2 Xiao Lv,2 Baojun Xiao,2 Yong Feng2 1Department of Rehabilitation, Wuhan No.1 Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, People’s Republic of China; 2Department of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, People’s Republic of China*These authors contributed equally to this workCorrespondence: Baojun Xiao; Yong Feng, Email drxiao999@sohu.com; fengyong@hust.edu.cnBackground: Histone deacetylase 9 (HDAC9) is a member of the HDAC gene family that plays essential roles in the organization of transcriptional regulation by catalyzing deacetylation of histone proteins. However, the effects of HDAC9 on osteonecrosis of femoral head (ONFH) have not been investigated. The present study aimed to reveal whether histone deacetylase 9 (HDAC9) regulated osteogenic differentiation.Methods: A lentiviral knockdown HDAC9 model was established in hBMSCs. Osteoblast-specific gene expression, such as Runx2, OCN was examined by qRT-PCR and Western blot, respectively. Though transcriptome sequencing and enrichment analysis, related signal pathways caused by down-regulation of HDAC9 were screened. The effect of HDAC9 on MAPK signaling pathway was determined by Western blot. Eventually, tert-Butylhydroquinone (tBHQ) was used to examine the effect of MAPK activation on osteogenesis in HDAC9 knockdown hBMSCs.Results: A lentiviral knockdown HDAC9 model was successfully established in hBMSCs. HDAC9 knockdown significantly inhibited osteoblast-specific gene expression, such as runt-related transcription factor 2 (Runx2), osteocalcin (OCN) and mineral deposition in vitro. Moreover, a total of 950 DEGs were identified in HDAC9-knockdown hBMSCs. We discovered that the MAPK signaling pathway might be related to this process by pathway enrichment analysis. HDAC9 knockdown signi